11/65. Area-selective stimulus-provoked seizures in post-anoxic coma. We describe the case of a 70-year-old patient in whom hemiconvulsive seizures occurred during metabolic derangement, multiple stroke and post-anoxic coma following cardiac arrest. We employed the methods of clinical and EEG evaluation and CT brain scan. We found that hemiconvulsive seizures were provoked following a light tactile stimulus in the left-trigeminal area and occasionally a strong tapping in the right-trigeminal area. We conclude that this type of stimulus-provoked seizure is extremely rare and could be explained by diffuse and severe brain damage. ( info) |
| Acute hepatic encephalopathy is a poorly defined syndrome of heterogeneous aetiology. We report a 49-year-old woman with alcoholic cirrhosis and hereditary haemorrhagic telangiectasia who developed acute hepatic coma induced by severe gastrointestinal bleeding. Laboratory analysis revealed excessively elevated blood ammonia. MRI showed lesions compatible with chronic hepatic encephalopathy and widespread cortical signal change sparing the perirolandic and occipital cortex. The cortical lesions resembled those of hypoxic brain damage and were interpreted as acute toxic cortical laminar necrosis. ( info) |
| The aim of the present study was to demonstrate the usefulness of fetal magnetic resonance imaging (MRI) in ischemic brain injury. We report seven cases of fetal brain ischemia prenatally suspected on ultrasound (US) and confirmed by fetal MRI. Sonographic abnormalities included ventricular dilatation (n=3), microcephaly (n=1), twin pregnancy with in utero death of a twin and suspected cerebral lesion in the surviving co-twin (n=3). MRI was performed with a 1.0 T unit using half-Fourier acquisition single-shot turbo spin-echo (HASTE) sequences between 28 and 35 weeks of gestation. US and MRI images were compared with pathologic findings or postnatal imaging. MRI diagnosed hydranencephaly (n=1), porencephaly (n=2), multicystic encephalomalacia (n=2), unilateral capsular ischemia (n=1), corpus callosum and cerebral atrophy (n=1). In comparison with US, visualization of fetal brain anomalies was superior with MRI. The present cases demonstrate that MRI is a valuable complementary means of investigation when a brain pathology is discovered or suspected during prenatal US. ( info) |
14/65. Hypoxic brain damage after intramuscular self-injection of diclofenac for acute back pain. We present a case of hypoxic brain damage that occurred after intramuscular injection of diclofenac due to a severe anaphylactic reaction. A 38-year-old nurse treated herself for acute lower back pain with 100 mg diclofenac intramuscularly. Five minutes later, she collapsed and developed coma and respiratory arrest. After cardiopulmonary resuscitation she was transferred to hospital. On admission she was comatose and received controlled ventilation of the lungs. magnetic resonance imaging and computerized tomography showed signs of hypoxic brain injury and the patient died from central cardiopulmonary failure 7 days later. Intramuscular treatment with non-steroidal anti-inflammatory drugs such as diclofenac has rare but potentially severe side-effects. Therefore, intramuscular injections are inappropriate and should be replaced with oral or rectal treatment, which has similar absorption profiles. ( info) |
15/65. time course of changes in diffusion-weighted magnetic resonance imaging in a case of neonatal encephalopathy with defined onset and duration of hypoxic-ischemic insult. The onset and duration of hypoxic-ischemic (HI) insults rarely can be determined precisely in perinatal asphyxia. The need to establish the timing of HI insults will be critical for the successful application of evolving neuroprotective therapies that may be administered to the asphyxiated newborn. diffusion-weighted magnetic resonance imaging has emerged as an imaging technique that can be used to identify HI brain injury before the detection of abnormalities by conventional magnetic resonance imaging. This case illustrates the early changes in diffusion-weighted and conventional magnetic resonance imaging studies and in quantitative values of the apparent diffusion coefficient in a unique case of neonatal asphyxia in which the onset and duration of the HI insult were known.hypoxia-ischemia, newborn brain, perinatal asphyxia, diffusion-weighted imaging, proton magnetic resonance spectroscopy. ( info) |
16/65. Acute pancreatic damage associated with convulsive status epilepticus: a report of three cases. Three cases involving a previously unreported association of acute pancreatic damage following convulsive status epilepticus (SE) are presented. A review of literature failed to reveal a similar association between SE and acute pancreatic damage. As possible pathophysiological mechanisms of this so far unknown sequel of SE, increased intraduodenal pressure during SE leading to the reflux of the duodenal contents into the pancreatic duct, along with altered metabolism of oxygen-derived free radicals during a prolonged seizure with hypoxia and ischemia resulting in acinar cell injury are suggested. We believe that SE should be considered as an additional risk factor of acute pancreatitis and that pancreatic enzymes should be monitored in patients who have prolonged seizures. ( info) |
17/65. Cochleosaccular pathology after perinatal and postnatal asphyxia: histopathologic findings. OBJECTIVE: This study describes the histopathologic findings of a patient with severe bilateral sensorineural hearing loss after perinatal and postnatal hypoxia and asphyxia. STUDY DESIGN: Histopathologic examination on the temporal bones. SETTING: The study was performed at the Elizabeth McCullough Knowles Otopathology Laboratory, Division of Otopathology, Department of otolaryngology, University of Pittsburgh School of medicine, Pittsburgh, PA, USA. RESULTS: Histopathologic examination on the left temporal bone revealed severe atrophy of the organ of corti throughout the entire cochlea, decrease in the number of the spiral ganglion cells especially in the basal turn, and mild atrophy of saccular macula. In the right temporal bone, similar abnormalities were observed in the inner ear, but the changes were milder than those in the left temporal bone. No other distinct pathologic finding was observed in either ear. CONCLUSION: These findings suggest that the presence of severe hypoxic ischemia causes cochleosaccular atrophy. To our knowledge, this is the first histopathologic case report describing the long-term effect of perinatal and postnatal hypoxia and asphyxia that produced cochleosaccular abnormalities in the human inner ear. ( info) |
18/65. Pseudo-subarachnoid hemorrhage of the head diagnosed by computerized axial tomography: a postmortem study of ten medical examiner cases. In this report, we describe ten cases of pseudo-subarachnoid hemorrhage on computer axial tomography (CT) scan of the head. A pseudo-subarachnoid hemorrhage is a false positive finding by CT of the head in which the scan is interpreted as being positive for a subarachnoid hemorrhage not substantiated by subsequent neuropathologic findings. This study is a retrospective review of postmortem cases brought into the Office of the Chief Medical Examiner for the State of maryland over a three-year period (from 1997 to 2000). We compared the clinician's impression of the CT scan with the postmortem neuropathology. The clinical diagnosis of subarachnoid hemorrhage was based on misinterpretation of non-contrast CT scans of the head. In six of the ten cases, the reading was performed by a radiologist and in four cases by nonradiologist physicians (emergency room physician, neurologist, or neurosurgeon). All the patients survived between a few hours to a few days after being admitted to the hospital. For most of the cases (80%), the neuropathology showed hypoxic/ischemic encephalopathy. The most common cause of death (four out of ten cases) was narcotic intoxication. This report is submitted so that clinicians and pathologist become more familiar with this entity. ( info) |
19/65. Effects of acute hypoxemia/ischemia on EEG and evoked responses at normothermia and hypothermia in humans. BACKGROUND: hypothermia is used clinically to prevent neurologic injury but the degree of protection which it affords at various levels of the nervous system in humans is difficult to establish. MATERIAL/methods: The temporal changes in EEG amplitude and somatosensory evoked potential (SEP) amplitudes in a patient experiencing acute normothermic hypoxemia, a patient experiencing acute circulatory arrest at moderate hypothermia and a collection of patients undergoing deep hypothermic circulatory arrest were analyzed to determine the rate at which changes occur during acute lack of oxygen delivery at various temperatures. RESULTS: In each case, it was found that more rostrally generated potentials disappeared more quickly than more peripheral potentials. All potentials decayed more slowly during acute normothermic hypoxemia than during circulatory arrest. During circulatory arrest at 14.4 degrees C, the amplitude of the Erb's point, N13 and N18 potentials in the SEP took 5 times longer to drop to 50% of their value at the onset of ischemia than with circulatory arrest at 30.9 degrees C. CONCLUSIONS: The longer times to disappearance of the SEP potentials during deep hypothermia compared to moderate hypothermia was consistent with the predicted 3.5-6.5 fold reduction in metabolic activity at deep hypothermia compared to moderate hypothermia. The prolonged time to disappearance of the SEP during normothermic hypoxemia demonstrates that even with reduced oxygen delivery the continued delivery of metabolic substrate can be critical to neural function. ( info) |
20/65. diffusion MRI in three types of anoxic encephalopathy. We report the clinical and diffusion-weighted MRI (DWI) features of three patients with different types of anoxic brain injury: attempted hanging (hypoxic hypoxia), carbon monoxide poisoning (histotoxic hypoxia), and hanging with cardiac arrest (hypoxic-ischemic encephalopathy, HIE). The first two patients, but not the third, recovered substantial neurological function. The distribution of DWI abnormalities was different and correlated well with the distinct neuropathological features of these entities. The prognosis after anoxic encephalopathy depends on the underlying mechanism and its severity, which may be reflected by DWI abnormalities. ( info) |